[Effect of swimming training on the expression of PKC δ/p66Shc protein in mouse myocardium].

To investigate the effects of different intensity of swimming training on p66Shc protein in mouse myocardium. Fifty Kunming mice were randomly divided into control group (Group C), weight-bearing swimming group (Group E), weight-bearing swimming + drug group (Group ER), non weight-bearing swimming group (Group P), non weight-bearing swimming + drug group (Group PR), with 10 mice in each group. Group C did not exercise. Groups E, ER, P, and PR received swimming training for 4 weeks. Groups E and ER performed weight-bearing swimming with a 3% body weight, and Group P and Group PR were swimming without weight-bearing, 60 min/d, 6 times/w. Mice in ER and PR groups were injected intraperitoneally with Rottlerin (0.3 mg/kg), a PKCδ inhibitor, before the last two exercises. Groups C, E, and P were injected with the same dose of normal saline. Samples were collected after training finished for 24 hours. The protein expressions of PKCδ, P-PKCδ, P66Shc, P-P66shc and NOX2 were detected by Western blot; PKCδ and P66Shc were detected by immunoprecipitation; malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) in myocardium and serum were analyzed by biochemistry. Compared with Group C, the protein expressions of PKCδ, P-PKCδ, P66Shc, P-P66shc and NOX2 in Group E were increased significantly (＜ 0.01), the serum and myocardial MDA levels, myocardial ROS were increased significantly (＜0.05 or ＜0.01), and the myocardial SOD activity was decreased (＜0.01), the PKCδ, P-PKCδ, P-P66shc and NOX2 in Group P were increased significantly (＜0.05 or ＜0.01), and the myocardial SOD activity was enhanced (＜0.05). Compared with Group E, the protein expressionS of PKCδ (＜0.01), P-PKCδ (＜0.01), P66Shc (＜0.05), P-P66shc (＜0.01), NOX2 (＜0.05) in Group ER was decreased significantly, the protein expression of P66Shc in Group P was decreased significantly (＜0.05), the myocardial MDA (＜0.01) and ROS (＜0.05) were decreased, and the activity of SOD was enhanced (＜0.01). Compared with Group P, the protein expressions of PKCδ, P-PKCδ and P-P66shc in Group PR were decreased significantly (＜0.01), while the expression of NOX2 was increased (＜0.05). Both swimming training of two intensities promoted the increase of PKCδ protein and its phosphorylation in mouse cardiomyocytes. High-intensity swimming training could significantly enhance the expression and phosphorylation level of p66Shc protein, resulting in the production of ROS and the decrease of antioxidant enzyme activity. Low-intensity swimming training enhanced the phosphorylation of p66Shc, but did not promote its protein expression, resulting in the enhancement of myocardial antioxidant capacity and exercise adaptation.